Time course of UVA‐ and UVB‐induced inflammation and hyperalgesia in human skin

Abstract

Dose-dependency and time course of hyperalgesia and erythema following UVA (16.8 and 36 J/cm(2)) and UVB (one and three times the minimum erythema threshold) irradiation was investigated in 10 healthy human subjects. Skin patches (1.5 cm in diameter) on the ventral side of the upper leg were irradiated with UVA or UVB light. Hyperaemia (Laser Doppler flowmetry, infrared thermography), thermal hyperalgesia to radiant heat stimuli, and mechanical hyperalgesia to controlled impact stimuli were tested at 1, 6, 12, 24, 48 and 96 h after irradiation. Dose-dependent delayed hyperaemia and hyperalgesia was induced only by UVB irradiation. UVB-induced increase in blood flow peaked at 12 h after irradiation and normalized by 96 h. Although superficial blood flow, as measured by Laser Doppler flowmetry, increased up to eight-fold, no significant increase of skin temperature was detected using infrared thermography. Development of mechanical and thermal hyperalgesia was delayed and reached a plateau between 24 and 48 h. In contrast to UVB, UVA irradiation of up to 36 J/cm(2), sufficient to produce intense tanning of the skin, did not induce significant hyperalgesia or delayed hyperaemia. It is concluded that UVB- but not UVA-irradiation is a suitable experimental model of subacute thermal and mechanical hyperalgesia. The different time courses of erythema and hyperalgesia indicate that inflammatory mediators responsible for vasodilatation are not identical with those inducing hyperalgesia. Copyright 1999 European Federation of Chapters of the International Association for the Study of Pain.

A novel model of inflammatory pain in human skin involving topical application of sodium lauryl sulfate

“…Subacute or long-lasting human hyperalgesia models are probably more relevant for studies of the mechanisms that underlie inflammatory or neuropathic pain. The limited human models available include UVB-inflammation [16,17], thermal injuries elicited by contact-heat [13] and freezing [18,19], and noninflammatory hyperalgesia induced by nerve growth factor [20]. The results of our study indicate that SLS-induced inflammation may be a novel model of inflammatory pain.…”

“…Comparisons across individual trials can be questionable. For example, inflammatory reactions induced by three times the minimal erythema dose of UVB in healthy subjects measured by laser Doppler flowmetry, as well as the presence and/or magnitude of secondary hyperalgesia, have shown quite different results in trials of apparently similar design [16,25,37]. However, comparative studies with several skin models may be relevant in the search for pivotal mediators of hyperalgesia in the skin during the life cycle of inflammation.…”

Central mechanisms of experimental and chronic neuropathic pain: Findings from functional imaging studies

“…parecoxib and acetylsalicylic acid (ASA) by using the UV-B model [42]. In contrast to other surrogate models the UV-B model has the advantage of an extended time frame in which hyperalgesia can be investigated [32,35]. Previous psychophysical studies have demonstrated antihyperalgesic and analgesic effects of non-steroidal anti-inflammatory drugs (NSAIDs) in this model [33,43].…”

“…UV-B model. To compare brain activations of different submodalities of hyperalgesia, Seifert and colleagues [31] induced both heat and mechanical hyperalgesia, using the UV-burn model [32,33] in healthy volunteers. An advantage of the UV-B model is that the induced hyperalgesia is stable over many hours, broadly follows intensity of the erythema and does not extend beyond the irradiated area, so that at least by the use of small radiated areas the resulting hyperalgesia is highly localized to the area of inflammation [34], although greater radiated areas are reported to induce relevant secondary hyperalgesia [35].…”

Representation of UV‐B‐induced thermal and mechanical hyperalgesia in the human brain: A functional MRI study

“…However, often only one submodality of stimulus-evoked pain, e.g., mechanical or thermal, has been investigated or primary and secondary hyperalgesia have been compared . Therefore, to compare brain activations of different submodalities of hyperalgesia, we induced both heat and mechanical hyperalgesia, using the UV-burn model [Bickel et al, 1998;Hoffmann and Schmelz, 1999] in healthy volunteers. The resulting areas of mechanical and heat hyperalgesia allowed us to compare the brain processing of both conditions directly and at balanced intensities.…”